Chapter 8 Cardiac Pathology Flashcards

1
Q

What is the most common cause of Ischemic Heart Disease and what are the risk factors?

A

Atherosclerosis. Risk factors are similar to those of atherosclerosis; incidence increases with age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is stable angina?

A

chest pain that arises with exertion or emotional distress, does not occur at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is stable angina due to?

A

atherosclerosis of coronary arteries with >70% stenosis; decreased blood flow is not able to meet the metabolic demands of the myocardium during exertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does stable angina represent?

A

reversible injury to myocytes ( no necrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is a hallmark sign of reversible cell damage?

A

cell swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does stable angina present?

A

chest pain (lasting <20 min) that radiates to the left arm or jaw, diaphoresis, and shortness of breath.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does EKG show with stable angina?

A

ST-segment depression due to subendocardial ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What relieves stable angina?

A

Rest or nitroglycerin (decreases preload)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is unstable angina?

A

chest pain that occurs at rest (still reversible)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is unstable angina usually due to?

A

rupture of an atherosclerotic plaque with thrombosis and INCOMPLETE occlusion of a coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What type of injury does unstable angina represent?

A

reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does EKG show in unstable angina?

A

ST-depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What relieves unstable angina?

A

nitro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does unstable angina carry a high risk for?

A

progression to MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Prinzmetal angina?

A

episodic chest pain unrelated to exertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is prinzmetal angina due to?

A

vasospasm of coronary artery (completely shuts it)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What type of injury does prinzmetal angina represent?

A

reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does EKG show in prinzmetal angina?

A

ST segement elevation due to transmural ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What relieves prinzmetal angina?

A

Nitro or Ca channel blockers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What type of cell injury occurs in MI?

A

necrosis of myocytes which is irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is usually the cause of MI?

A

rupture of an atherosclerotic plaque with thrombosis and COMPLETE occlusion of a coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are some other causes of MI? (3)

A

coronary artery vasospasm (due to prinzmetal angina or cocaine use)
Emboli
Vasculitis (Kawasaki disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the clinical features of an MI?

A

severe crushing chest pain (lasting >20 min) that radiates to left arm or jaw, diaphoresis, and dyspnea (due to pulmonary congestion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How are each of the four chambers of the heart usually affected in an MI?

A

Infarction usually incolves the LV: RV,RA,LA are generally spared.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What does occlusion of the LAD lead to in MI?

A

infarction of the anterior wall and anterior septum of the LV; LAD is most commonly involved artery in MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What does occlusion of the RCA cause in MI?

A

leads to infarction of the posterior wall, posterior septum, and papillary muscles of the LV: RCA is the second most commonly involved artery in MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What does occlusion of the left circumflex artery cause in MI?

A

infarction of the lateral wall of the LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What portions of the wall are damaged initially in MI and what does EKG show?

A

Initially subendocardial necrosis involving less than 50% of the wall leads to ST-depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What portions of the wall become damages with continued ischemia in an MI and what EKG changes are seen?

A

transmural necrosis involving most of the myocardial wall causing ST-elevation on EKG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What two cardiac enzymes become elevated in MI?

A

Troponin I and CK-MB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Describe the time course and level of troponin I after an MI?

A

Troponin I is the most sensitive and specific marker for MI. levels rise 2-4 hours after infarction, peak at 24 hours, and return to normal by 7-10 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

describe the time course and level of CK-MB after an MI?

A

CK-MB is used for detecting reinfarction that occurs days after an initial MI. levels rise in 4-6 hours, peak at 24, and return to normal by 72.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Name 6 pharmacological treatments of MI

A

1 ASA and/or Heparin - limits thrombosis
2 Supplemental oxygen - minimizes ischemia
3 Nitrates - vasodilate veins and coronary arteries
4 BB slows HR, decreasing oxy demand and risk for arrhythmia
5 ACE-I decreases LV dilation
6 Fibrinolysis or angioplasty- opens blocked vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What does reperfusion of ireversibly damaged cells cause?

A

can result in calcium influx, leading to hypercontraction of myofibrils (Contraction band necrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Describe reperfusion injury and how this would show up in labs?

A

Return of oxygen and inflammatory cells may lead to free radical generation further damaging myocytes. Cardiac enzymes would continue to rise even after opening blocked vessels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the gross and microscopic changes and complications from 0-4 hours following an MI?

A

Gross- NONE
Microscopic - NONE
Complications- Cardiogenic shock (massive infarction), CHF, arrythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the gross and microscopic changes and complications from 4-24 hours following an MI?

A

Gross- Dark discoloration
microscopic - coagulative necrosis
complications- arrhythmia (if it doesnt happen by now it probably wont happen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the gross and microscopic changes and complications from 1-3 days following an MI?

A

Gross- yellow pallor
microscopic- neutrophils
complications - fibrinous pericarditis (only with transmural injury); presents as chest pain with friction rub

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the gross and microscopic changes and complications from 4-7 days following an MI?

A

Gross - yellow pallor
microscopic - macrophages
complications - this is the time when the wall is the weakest. rupture of ventricular free wall (leads to cardiac tamponade), interventricular septum (leads to shunt), or papillary muscle (leads to mitral insufficiency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the gross and microscopic changes and complications from 1-3 weeks following an MI?

A

Gross - red border emerges as granulation tissue enters from edge of infarct.
microscopic - granulation tissue with plump fibroblasts, collagen, and BV
complications - none in chart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the gross and microscopic changes and complications in the months following an MI?

A

gross - white scar (weaker than healthy tissue)
microscopic - fibrosis
complications - aneurysm, mural thrombus, or Dressler syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is Dressler syndrome?

A

autoimmune pericarditis due to antigen exposure after an MI usually 6-8 weeks post infarct.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is Sudden cardiac death? what usually causes it?

A

Unexpected death due to cardiac disease: occurs without symptoms or <1 hours after symptoms arise. usually due to fatal ventricular arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the most common etiology of sudden cardiac death?

A

acute ischemia; 90% of patients have preexisting severe atherosclerosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are some less common causes of sudden cardiac death?

A

mitral valve prolapse, cardiomyopathy, and cocaine abuse (vasospasm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is chronic ischemic heart disease? What does it progress to?

A

Poor myocardial function due to chronic ischemic damages (with or without infarction); progresses to CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are 5 causes of left-sided heart failure?

A

1 ischemia
2 hypertension leads to concentric hypertrophy, thicker wall, more difficult to fill
3 dilated cardiomyopathy
4 MI
5 restrictive cardiomyopathy (cant fill heart appropriately)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are clinical features of left sided heart failure due to?

A

decreased forward perfusion and pulmonary congestion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What does pulmonary congestion lead to in left sided heart failure?

A

leads to pulmonary edema.
results in dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and crackles. Small congested arteries may burst, leading to intraaleolar hemorrhage; marked by hemosiderin-laden macrophages (heart failure cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the consequence of decreased forward perfusion in left sided heart failure?

A

decreased flow to kidneys leads to activation of RAS system. Fluid retention exacerbates CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the mainstay of treatment for left sided heart failure?

A

ACE-I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the most common cause of right sided heart failure and what are two other causes?

A

most common is left sided heart failure. other important causes include left-to-right shunt and chronic lung disease (cor pulmonale) - develop hypoxia, vessels constrict, pulmonary pressure and resistance increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are clinical features of right sided heart failure due to?

A

congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the clinical features of right sided heart failure?

A

JVD
painful hepatospenlomegaly with characteristic ‘nutmeg’ liver; may lead to cardiac cirrhosis
dependent pitting edema due to increased hydrostatic pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

When do congenital heart defects arise and what percent of live births are they seen in? are they mainly sporadic or inherited?

A

Arise during embryogenesis (usually weeks 3-8); seen in 1% of live births, most are sporadic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What do congenital cardiac defects often result in?

A

Shunting between the left (systemic) and right (pulmonary) circulations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Describe how the reversal of a left to right shunt occurs?

A

increased flow through th epulmonary circulation results in hypertrophy of pulmonary vessels and pulmonary hypertension. Increased pulmonary resistance eventually results in reversal of shunt, leading to late cyanosis (Eisenmenger syndrome) with right ventricular hypertrophy, polycythemia and clubbing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How do defects with right to left shunting present?

A

usually as cyanosis shortly after birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is a ventricular septal defect and what is it associated with?

A

Defect in the septum that divides the right and left ventricles. Most common congenital heart defect. associated with fetal alcohol syndrome.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What does a VSD result in? comment of the effects of the size of the defect.

A

a left to right shunt. The size of the defect determines the extent of the shunting and age at presentation. Small defects are often asymptomatic; large defects can lead to eisenmenger syndrome.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What does treatment of a VSD involve?

A

surgical closure; small defects may close spontaneously.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is an atrial septal defect? what is the most common type?

A

defect in the septum that divides the right and left atria; most common type is ostium secundum (90%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is ostium primum associated with?

A

Down Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What does ASD result in? How can it be detected on examination.

A

left to right shunt and split S2 on auscultation (Increased blood in right heart delays closure of the pulmonary valve

65
Q

What is an important complication of ASD?

A

paradoxical emboli - crosses to left heart and lodges in systemic circulation.

66
Q

What is a patent ductus arteriosus and what is it associated with?

A

failure of ductus arteriosus to close; associated with congenital rubella.

67
Q

Where is the a PDA wrt the major branches of the aorta?

A

below the major branches

68
Q

What does PDA result in?

A

left to right shunt between the aorta and the pulmonary artery.

69
Q

Describe the symptoms and signs of a PDA?

A

Asymptomatic at birth with continuous ‘machine-like’ murmur; may lead to eisenmenger syndrome, resulting in lower extremity cyanosis.

70
Q

What does treatment of a PDA involve?

A

indomethacin, which decreases PGE, resulting in PDA closure

71
Q

What is the tetrology of fallot?

A

1 stenosis of the right ventricular outflow tract
2 right ventricular hypertrophy
3 VSD
4 an aorta that overrides the VSD

72
Q

What does tetrology of fallot lead to?

A

right to left shunt leads to early cyanosis; degree of stenosis determines the extent of shunting and cyanosis

73
Q

What are some methods patients learn to respond to a cyanotic spell with tetrology of fallot?

A

learn to squat which increases arterial resistance and decreases shunting and allows more blood to reach lungs

74
Q

What can be seen on X-ray in tetrology of fallot?

A

‘boot-shaped’ heart

75
Q

What is transposition of the great arteries?

A

Characterized by pulmonary artery arising from the left ventricle and aorta arising from the right ventricle.

76
Q

What is transposition of the great arteries associated with?

A

maternal diabetes

77
Q

What does transposition of the great arteries present with?

A

early cyanosis; pulmonary and systemic circuits do not mix.

78
Q

What does treatment of transposition of the great arteries entail?

A

Creation of a shunt after birth is required for survival.

PGE can be administered to maintain a PDA until definitive surgical repair is performed.

79
Q

What cardiac changes does transposition of the great arteries result in?

A

hypertrophy of the right ventricle and atrophy of the left ventricle

80
Q

What is truncus arteriosus?

A

Characterized by a single large vessel arising from both ventricles. truncus fails to divide

81
Q

How does truncus arteriosus present?

A

presents with early cyanosis; deoxygenated blood from right ventricle mixes with oxygenated blood from left ventricle before pulmonary and aortic circulations separate

82
Q

What is tricuspid atresia? what is seen in the RV?

A

tricuspid valve oriface fails to develop; right ventricle is hypoplastic

83
Q

What is tricuspid atresia often associated with, what does it result in, and how does it present?

A

often associated with ASD, resulting in a right to left shunt; presents with early cyanosis

84
Q

What is coarctation of the aorta? what two forms is it generally split into?

A

narrowing of the aorta; classically divided into infantile and adult forms

85
Q

What is infantile coarctation of the aorta associated (congenital defect) with and where does it usually occur?

A

Associated with a PDA, lies after the aortic arch but before the PDA

86
Q

How does infantile coarctation of the aorta present and what is it associated with (inherited disease)?

A

Presents as lower extremity cyanosis in infants, often at birth. is associated with Turner syndrome

87
Q

Is adult coarctation of the aorta associated with a PDA and where does it lie? What other deformity is it associated with?

A

is NOT associated with a PDA and lies distal to aortic arch. associated with a bicuspid aortic valve

88
Q

How does adult coarctation of the aorta present?

A

presents as HTN in the upper extremities and hypotension with weak pulses in the lower extremities; classically discovered in adulthood

89
Q

What signs can be seen on xray in aortic coarctation and what is this due to?

A

collateral circulation develops across the intercostal arteries; engorged arteries cause ‘notching’ of ribs on x-ray.

90
Q

What do valvular lesions generally result in?

A

stenosis or regurgitation

91
Q

What is acute rheumatic fever a complication of? who does it usually affect?

A

systemic complication of pharyngitis due to group A beta hemolytic streptococci; affects children 2-3 weeks after an episode of streptococcal pharyngitis

92
Q

What is Acute rheumatic fever caused by molecularly?

A

caused by molecular mimicry ; bacterial M protein resembles human tissue

93
Q

How is diagnosis made of acute rheumatic fever?

A

based on the jones criteria.
1 evidence of prior group A strep infection (elevated ASO or anti-DNase B titers)
2 minor criteria are nonspecific and include fever and elevated ESR
3 Major criteria

94
Q

What are the major criteria for acute rheumatic fever?

A
Migratory polyarthritis
pancarditis
subcutaneous nodules
erythema miarginatum
sydenham chorea
95
Q

What is migratory polyarthritis?

A

swelling and pain in a large joint that resolves within days and “migrates to involve another large joint.

96
Q

Describe the endocarditis in pancarditis of acute rheumatic fever?

A

mitral valve is involved more commonly than aortic valve. characterized by small vegetations along the lines of closure that lead to regurgitation

97
Q

describe the myocarditis in pancarditits of acute rheumatic fever?

A

myocarditis with aschoff bodies that are characterized by foci of chronic inflammation, reactive histiocytes with slender, wavy nuclei (Anitschkow cells), giant cells, and fibrinoid material; myocarditis is the most common cause of death during the acute phase

98
Q

What does pericarditis in acute rheumatic fever lead to?

A

leads to friction rub and chest pain

99
Q

What is erythema marginatum?

A

annular, nonpruritic rash with erythematous borders, commonly involving the trunk and limbs

100
Q

What is sydenham chorea?

A

rapid, involuntary muscle movements

101
Q

What is usually the result of an acute attack of rheumatic fever?

A

Acute attack usually resolves but may progress to chronic rheumatic heart disease; repeat exposure to group A strep results in relapse of the acute phase and increases risk for chronic disease.

102
Q

What is chronic rheumatic heart disease characterized by?

A

valve scaring that arises as a consequence of rheumatic fever

103
Q

What does chronic rheumatic heart disease result in? what valves are affected?

A

stenosis with a classic ‘fish mouth’ appearance.
almost always involves the mitral valve; leads to thickening of chordae tendinae and cusps. occasionally involves the aortic valve; leads to fusion of the commissures. other valves are less frequently involved

104
Q

What do complications of chronic rheumatic heart disease include?

A

infectious endocarditis

105
Q

What is aortic stenosis?

A

Narrowing of the aortic valve orifice

106
Q

What is aortic stenosis usually due to?

A

fibrosis and calcification from ‘wear and tear’

107
Q

When does aortic stenosis generally present and what increases the risk for it?

A

presents in late adulthood (>60 years). bicuspid aortic valve increases risk and hastens disease onset. A normal aortic valve has three cusps; fewer cusps results in increased ‘wear and tear’ on each remaining cusp

108
Q

What is an alternative way aortic stenosis can arises instead of ‘wear and tear’ how do you tell the two apart?

A

may also arise from chronic rheumatic valve disease; coexisting mitral stenosis and fusion of the aortic valve commissures distinguish rheumatic disease from ‘wear and tear’

109
Q

what does aortic stenosis lead to? How can it be detected on exam?

A

cardiac compensation leads to prolonged asymptomatic stage during which a systolic ejection click followed by a crescendo-decrescendo murmur is heard.

110
Q

What do complications of aortic stenosis include? 3

A

1 concentric left ventricular hypertrophy - may progress to cardiac failure
2 angina and syncope with exercise - limited ability to increase blood flow across the stenotic valve leads to decreased perfusion of the myocardium and brain.
3 microangiopathic hemolytic anemia

111
Q

What is the treatment of aortic stenosis and when is it done?

A

Treatment is valve replacement AFTER onset of complications

112
Q

What is Aortic Regurgitation?

A

backflow of blood from the aorta into th eleft ventricle during systole.

113
Q

What does aortic regurgitation arise due to?

A

aortic root dilation (eg. syphilitic aneurysm and aortic dissection) or valve damage (eg. infectious endocarditis); most common cause is isolated root dilation

114
Q

What are 3 clinical symptoms of aortic regurgitation?

A

1 early, blowing diastolic murmur
2 Hyperdynamic circulation due to increased pulse pressure
3 LV dilation and eccentric hypertrophy (due to volume overload)

115
Q

Describe the hyperdynamic circulation due to increased pulse pressure in aortic regurgitation?

A

diastolic pressure decreases due to regurgitation, while systolic pressure increases due to increased stroke volume. presents with bounding pulse (water-hammer pulse), pulsating nail bed (quincke pulse), and head bobbing

116
Q

What is mitral valve prolapse?

A

Ballooning of mitral valve into left atrium during systole

117
Q

What is mitral valve prolapse due to?

A

myxoid degeneration (accumulation of ground substance) of the valve, making it floppy

118
Q

What is the etiology of mitral valve prolapse and what syndromes is it associated with?

A

etiology is unknown; may be seen in marfan or ehlers danlos syndrome

119
Q

How does mitral valve prolapse present?

A

With an incidental mid-systolic click followed by a regurgitation murmur; usually asymptomatic

120
Q

What can cause the click and murmur of mitral valve prolapse to become softer?

A

Squatting increases systemic resistance and decreases left ventricular emptying.

121
Q

What complications are seen in mitral valve regurgitation?

A

complications are rare, but include infectious endocarditis, arrhythmias, and severe mitral regurgitation.

122
Q

What is treatment for mitral valve prolapse?

A

valve replacement

123
Q

What is mitral valve regurgitation?

A

reflux of blood from the left ventricle into the left atrium during systole

124
Q

What does mitral valve regurgitation arise as a complication of? 1 main and 4 others

A

usually mitral valve prolapse; other causes include LV dilatation (left sided heart failure) infective endocarditis, acute rheumatic heart disease, and papillary muscle rupture after a MI

125
Q

What are the clinical feature of mitral valve regurgitation?

A

holosystolic “blowing” murmur; louder with squatting (increased systemic resistance decreases LV emptying) and expiration (increases return to left atrium) results in volume overload and left sided heart failure.

126
Q

What is mitral stenosis, what is it usually due to?

A

narrowing of the mitral valve orifice usually due to chronic rheumatic valve disease

127
Q

What are the clinical feature of mitral stenosis?

A

1 Opening snap followed by a diastolic rumble

2 Volume overload leads to dilatation of the left atrium

128
Q

What does dilatation of the left atrium in mitral stenosis lead to?

A

1 pulmonary congestion with edema and alveolar hemorrhage
2 pulmonary hypertension and eventual right sided heart failure
3 atrial fibrillation with associated risk for mural thrombi

129
Q

What is endocarditis? What is it usually due to?

A

inflammation of the endocardium that lines the surface of cardiac valves; usually due to bacterial infection

130
Q

What is the most common overall cause of endocarditits, describe its virulence?

A

Streptoccocus Viridans, low virulence

131
Q

What is required for a strep viridans endocarditis, describe the vegetations?

A

Infects only previously damaged valves (eg chronic rheumatic heart disease and mitral valve prolapse). results in small vegetations that do not destroy the valve (SUBACUTE ENDOCARDITIS)

132
Q

Describe the pathophysiology of subacute endocarditis with strep viridans?

A

damaged endocardieal surface develops thrombotic vegetations (platelets and fibrin). Transient bacteremia leads to trapping of bacteria in the vegetations; prophylactic antibiotics decrease risk of endocarditis (dental exams)

133
Q

What is the most common cause of endocarditis in IV drug users, what valve is involved, and what does it result in?

A

Staph Aureus, high virulence organism that infects normal valves, most commonly the tricuspid. results in large vegetations that destroy the valve (ACUTE ENDOCARDITIS)

134
Q

What organism is associated with the endocarditis of prosthetic valves?

A

Staph epidermidis

135
Q

What organism is associated with endocarditis of patients with underlying colorectal carcinoma?

A

Strep Bovis

136
Q

What are the HACEK organisms and what is unique about the endocarditis they cause?

A

Haemopholus, Actinobacillus, Cardiobacterium, Eikenella, Klingella all are associated with endocarditis with negative blood cultures.

137
Q

What do clinical features of endocarditis include? 4

A

1 Fever - due to bacteremia
2 murmur - due to vegetations on heart valve
3 Janeway lesions (erythematous nontender lesions on palms and soles), Osler nodes (tender lesions on fingers and toes), splinter hemorrhages in nail bed, and roth spots in retina, all due to embolization of splinter hemmhorages
4 anemia of chronic disease

138
Q

What are the laboratory findings in endocarditis? 3

A

1 positive blood cultures
2 anemia of chronic disease (decreased Hb, decreased MCV, increased ferritin, decreased TIBC, decreased serum iron, decreased saturation
3 tranesophageal echocardiogram is useful for detecting lesions on valves

139
Q

Describe nonbacterial endocarditis

A

Sterile vegetations that arise in associated with a hypercoaguable state or underlying adenocarcinoma. Vegetations arise on the mitral valve along lines of closure and result in mitral regurgitation

140
Q

Describe libmann Sacks endocarditis

A

is due to steril vegetations that arise in association with SLE. Vegetations are present on the surface and undersurface of the mitral valve and result in mitral regurgitation.

141
Q

What is dilated cardiomyopathy?

A

Dilation of all four chambers of the heart; most common form of cardiomyopathy

142
Q

What does dilated cardiomyopathy result in?

A

Results in systolic dysfunction (ventricles cannot pump), leading to biventricular CHF; complications include mitral and tricuspid regurgitation and arrhythmia with sudden death, or heart failure. Dilated cardiomyopathy is a late complication.

143
Q

What is the most common cause of dilated cardiomyopathy?

A

idiopathic

144
Q

What are 6 other causes of dilated cardiomyopathy

A

1 Genetic mutation (usually autosomal dominant)
2 Myocarditis
3 Alcohol abuse
4 Drugs (Doxorubicin and cocaine)
5 Pregnancy - seen during late pregnancy or soon (weeks to months) after birth
6 Hemochromatosis

145
Q

What is the most common infectious agent causing myocarditis and a dilated cardiomyopathy and what is it characterized by? What are the symptoms

A

usually due to coxsackie A or B - characterized by a lymphocytic infiltrate in the myocardium; results in chest pain, arrhythmia with sudden death, or heart failure. Dilated cardiomyopathy is a late complication.

146
Q

What is the treatment for a dilated cardiomyopathy?

A

Heart Transplant

147
Q

What is hypertrophic cardiomyopathy?

A

massive hypertrophy of the left ventricle

148
Q

What is hypertrophic cardiomyopathy due to?

A

genetic mutations in sarcomere proteins; most common form is autosomal dominant

149
Q

What are the clinical features of hypertrophic cardiomyopathy? (3)

A

1 decreased CO- LV hypertrophy eads to diastolic dysfunction (ventricle cannot fill, loss of compliance)
2 Sudden death due to ventricular arrhythmias; hypertrophic cardiomyopathy is a common cause of sudden death in young athletes.
3 syncope with exercise - subaortic hypertrophy of the ventricular septum results in functional aortic stenosis.

150
Q

What does biopsy show in hypertrophic cardiomyopathy?

A

Shows myofiber hypertrophy with disarray

151
Q

What is restrictive cardiomyopathy?

A

Decreased compliance of the ventricular endomyocardium that restricts filling during diastole

152
Q

Name five causes of restrictive cardiomyopathy?

A
1 amyloidosis
2 sarcoidosis
3 endocardial fibroelastosis (Children)
4 Loeffler syndrome (endomyocardial fibrosis with an eosinophilic infiltrate with eosinophilia)
5 Hemochromatosis
153
Q

How does restrictive cardiomyopathy present?

A

CHF; classic finding is low-voltage EKG with diminished QRS amplitude

154
Q

What is myxoma?

A

Benign mesenchymal tumor with a gelatinous appearance and abundant ground substance on histology (most common primary cardiac tumor in adults)

155
Q

What is the appearance and symptoms of a myxoma?

A

Usually forms a pedunculated mass in the left atrium that causes syncope due to obstruction of the mitral valve

156
Q

What is a rhabdomyoma? Who is it most common in, and what is it associated with?

A

A benign hamartoma of cardiac muscle (most common primary cardiac tumor in children; associated with tuberous sclerosis)

157
Q

What is more common in the heart; metastatic tumors or primary tumors?

A

metastatic

158
Q

What are common metastases to the heart?

A

breast, lung carcinoma, melanoma, lymphoma

159
Q

What do mets to the heart most commonly involve, and what results?

A

the pericardium; resulting in a pericardial effusion.